Nutritive Sweeteners Research Articles

Low and no calorie sweeteners (LNCS); myths and realities.

Since their introduction in the market, there has been much debate regarding the health effects of low and no calorie sweetners (LNCS). Therefore, through this review, we aim to establish scientific information about the most commonly used LNCS by the food industry. Key questions about uses, safety, and weight control are reviewed. Scientific evidence revised concludes that LNCS available on the market are safe and no epidemiological relationship has been established with the development of non-communicable diseases, including different kind of cancer in humans. Also, LCNS combined with physical activity and a healthy lifestyle can play a significant role in weight loss and the maintenance of a healthy weight. But non nutritive sweeteners will be helpful only as long as people don't eat additional calories later as compensation. Even more, LNCS represent an additional instrument in the dietary treatment of people with diabetes for metabolic control, without avoiding sweet taste.

Nonnutritive sweeteners are not supernormal stimuli.

BackgroundIt is often claimed that non-nutritive sweeteners (NNS) are ‘sweeter than sugar’, with the implicit implication high potency sweeteners are super-normal stimuli that encourage exaggerated responses. This study aimed to investigate the perceived sweetness intensity of a variety of nutritive (Sucrose, Maple Syrup, and Agave Nectar) and NNS (Acesulfame-K (AceK), Rebaudioside A (RebA), Aspartame, and Sucralose) in a large cohort of untrained participants using contemporary psychophysical methods.MethodsParticipants (n=401 total) rated the intensity of sweet, bitter, and metallic sensations for nutritive and NNS in water using the general labeled magnitude scale (gLMS).ResultsSigmoidal Dose-Response functions were observed for all stimuli except AceK. That is, sucrose follows a sigmoidal function if the data are not artifactually linearized via prior training. More critically, there is no evidence that NNS have a maximal sweetness (intensity) greater than sucrose; indeed, the maximal sweetness for AceK, RebA and Sucralose were significantly lower than for concentrated sucrose. For these sweeteners, mixture suppression due to endogenous dose-dependent bitter or metallic sensations appears to limit maximal perceived sweetness.ConclusionsIn terms of perceived sweetness, non-nutritive sweeteners cannot be considered super-normal stimuli. These data do not support the view that non-nutritive sweeteners hijack or over-stimulate sweet receptors to product elevated sweet sensations.

Consumer knowledge of non‐nutritive sweeteners (1020.6)

Consumer knowledge of artificial/non‐nutritivesweeteners (NNS) is incompletely understood. NNS can be identified by chemical name (CN) and trade name (TN). An online survey addressing NNS knowledge was sent to 1630 university subjects with 720 completing it in 5.00 ± 0.01 min. When asked to write a NNS definition, respondents included 1.15 ± 0.99 out of four reference components. Definition score was highly correlated (p<0.0001) with ACT score, food ingredient label use, and prior nutrition education, but not BMI, gender, or attempted weight loss history. When asked to provide examples from memory, respondents could name 1.23 ± 1.07 NNS; 1.09 ± 1.0 were by TN and 0.14 ± 0.45 were by CN. A randomized click‐drag‐box was used to examine word recognition success within five categories (TN, CN, nutritive sweetener, nutrient, and decoy NNS name) containing seven examples within each category. NNS identification of TN was >60% for Sweet’N Low, Splenda, Sweet One, NutraSweet, Equal, and Stevia. No CNs, nutritive sweeteners, or nutrients were identified by >60% of respondents as NNS. Three of seven decoy NNS names were thought to be real NNS by >60% of respondents. This study demonstrates that consumers are less able to identify NNS by CN than by TN. Food ingredient labeling uses CN, therefore, consumers are inadequately equipped to know if they consume NNS in their daily diet.

Chronic intake of honey, sugar and high fructose corn syrup exert equivalent effects on glucose and insulin (1039.4)

Consumption of nutritive sweeteners is high with added sugars’ intake from the WWEIA (2009‐2010) survey in all individuals 蠅 2 yr at 76.2 g or 295 kcal daily. Controversy continues regarding the metabolic effects of the source of sweetener. Our goal was to evaluate the glycemic and insulin effect of chronic consumption of honey, sucrose, and high fructose corn syrup (HFCS 55). A randomized, crossover designed study compared glucose and insulin responses in overweight and obese adults (n=46). Participants underwent an OGTT at baseline and after 2 weeks of a daily dose of 50 g of the assigned sweetener. All participants were asked to not consume any other sweeteners throughout the trial. A 1‐2 week washout period was completed before cross‐over assignment to another nutritive sweetener. Body weight was measured and blood samples for the OGTT were obtained at 0, 15, 30, 60, 90 and 120 minutes and glucose and insulin concentrations determined. The incremental area under the curve (iAUC) for glucose and insulin was determined by trapezoidal rule. Outcome data were analyzed by repeated measures ANOVA. There were no statistically significant differences between or within treatment for glucose or insulin iAUC at baseline or post‐treatment. Body weight was unchanged by treatment. Chronic intake of honey, sugar and HFCS 55 exerted similar effects on glycemic and insulin responses assessed by OGTT in overweight and obese adults.

Sugar substitutes and health

The sugar substitutes also may also be called as alternative, artificial, high-intensity, or non- nutritive sweeteners, can replace the sweetness of sugar while providing few or no calories. In addition to the calorie savings, these sugar substitutes have the advantage of not promoting tooth decay, and they are useful in dietary planning for people who are coping with obesity or diabetes. Sugar substitutes includes both food ingredients with very strong sweetening power that provide zero or very few calories, which are used in very small amounts to sweeten foods, and bulk sweetening agents such as polyols, which can replace both the bulk of sugar and some of its sweetness. The availability of a variety of safe sugar substitutes is of benefit to consumers because it enables food manufacturers to formulate a variety of good-tasting sweet foods and beverages that are safe for the teeth and general health.

Abstract 359: Effects of Erythritol on Endothelial Function in People with Type 2 Diabetes Mellitus

Erythritol is a polyol compound used as a low calorie nutritive sweetener. Several animal model studies have shown that erythritol has antioxidant properties and may improve endothelial function. The goal of this pilot study was to obtain evidence for such an effect in patients with type 2 diabetes mellitus (DM). Vascular testing included brachial artery flow-mediated dilation (FMD), reactive hyperemia, digital peripheral arterial tonometry (EndoPAT), carotid-femoral pulse wave velocity (PWV), central pulse pressure, and brachial blood pressure. We also measured blood glucose, insulin, C-peptide, C-reactive protein and urine F2 isoprostanes. Twenty-four participants (age 56±5 yrs, 54% female) consumed erythritol as a flavored beverage (12g x3/day) for 28 days. We assessed the effect of erythritol on vascular function compared to baseline at three time points: Acute (2 hours after erythritol 24 g), chronic (at day 28), and acute-on-chronic (day 28 after erythritol 24g). We did not observe a significant change in brachial artery FMD or reactive hyperemia. Acute consumption of erythritol produced a significant improvement in endothelial function measured by EndoPAT (lnPAT ratio 0.52±0.48 vs. 0.87±0.29, P=0.005). lnPAT ratio was 0.72±0.33 (P=0.19 vs. baseline) after chronic consumption and 0.84±0.34 after acute-on-chronic consumption (P=0.02). Following 28 days of erythritol consumption we observed a favorable effect on markers of aortic compliance: significant reduction in central pulse pressure from 47±13 to 41±9 mmHg (P=0.021) and strong trend for decreased PWV from 9.1±1.4 to 8.6±1.6 cm/sec (P=0.06). Markers of glucose metabolism, oxidative stress and inflammation did not vary throughout the study. We observed a trend for reduced systolic blood pressure after chronic erythritol consumption (131±16 to 128±11 mmHg, P=0.10). A subgroup analysis of 12 patients with systolic blood pressure above 130 mmHg yield a significant reduction in systolic blood pressure from 144±12 to 133±9 mmHg (P=0.01). This pilot study suggests that erythritol may have favorable effects on small vessel endothelial function, blood pressure, and central aortic stiffness in DM patients. Confirmation of these findings will require a placebo-controlled study.

A randomized, crossover comparison of the effects of high fructose corn syrup versus sucrose intake on basic physiologic measures

High fructose corn syrup (HFCS) has received growing attention and controversy in both popular and scientific media for its potential to differentially influence risk factors associated with metabolic syndrome, relative to sucrose (SUC). To date, no studies have examined the effects of acute ingestion of HFCS versus SUC on basic physiologic measures. The current study compared the effects of acute HFCS and SUC intake on blood pressure (BP), heart rate (HR), body temperature (BT) and blood glucose (BG) levels. Thirteen healthy, fasted men (n=3) and women (n=10) participated in a crossover design study, consuming caffeine‐free carbonated beverages (355mL) sweetened with either HFCS (37g) or SUC (37g) on separate days. BP, BT, HR, and BG were measured at baseline and 5min, 30min and 120min post‐consumption. A sweetener‐by‐time interaction (P = 0.02) was observed for HR, with mean 30min measures higher for HFCS (72 ± 3bpm) relative to SUC (65 ± 3bpm). Regardless of sweetener, BG was higher at 5min and 30min compared to baseline and 120min (P < 0.001); BT was lower at 5min compared to all other timepoints (P < 0.001). These data suggest the potential for a differential influence of sweetener type on HR and illustrate the effect of nutritive sweetener ingestion on BG and BT. Further study is warranted to establish the mechanistic basis for the observed effects.Supported by EMU URSP

Major Carbohydrate, Polyol, and Oligosaccharide Profiles of Agave Syrup. Application of this Data to Authenticity Analysis

Nineteen pure agave syrups representing the three major production regions and four processing facilities in Mexico were analyzed for their major carbohydrate, polyol, and oligosaccharide profiles, as well as their physicochemical properties (pH, °Brix, total acidity, percent total titratable acidity, and color). Additionally, the detection of intentional debasing of agave syrup with four commercial nutritive sweeteners (HFCS 55 and 90, DE 42 and sucrose) was afforded by oligosaccharide profiling employing both high performance anion exchange liquid chromatography with pulsed amperometric detection (HPAE-PAD) and capillary gas chromatography with flame ionization detection (CGC-FID). Results showed that the major carbohydrate and polyol in agave syrups were fructose and inositol with mean concentrations of 84.29% and 0.38%, respectively. Oligosaccharide profiling was extremely successful for adulteration detection with detection limits ranging from 0.5 to 2.0% for the aforementioned debasing agents. Also, all four of these possible adulterants could be detected within a single chromatographic analysis.

Altered processing of sweet taste in the brain of diet soda drinkers

Artificially sweetened beverage consumption has been linked to obesity, and it has been hypothesized that considerable exposure to nonnutritive sweeteners may be associated with impaired energy regulation. The reward system plays an integral role in modulating energy intake, but little is known about whether habitual use of artificial sweetener (i.e., diet soda consumption) may be related to altered reward processing of sweet taste in the brain. To investigate this, we examined fMRI response after a 12-hour fast to sucrose (a nutritive sweetener) and saccharin (a nonnutritive sweetener) during hedonic evaluation in young adult diet soda drinkers and non-diet soda drinkers. Diet soda drinkers demonstrated greater activation to sweet taste in the dopaminergic midbrain (including ventral tegmental area) and right amygdala. Saccharin elicited a greater response in the right orbitofrontal cortex (Brodmann Area 47) relative to sucrose in non-diet soda drinkers. There was no difference in fMRI response to the nutritive or nonnutritive sweetener for diet soda drinkers. Within the diet soda drinkers, fMRI activation of the right caudate head in response to saccharin was negatively associated with the amount of diet sodas consumed per week; individuals who consumed a greater number of diet sodas had reduced caudate head activation. These findings suggest that there are alterations in reward processing of sweet taste in individuals who regularly consume diet soda, and this is associated with the degree of consumption. These findings may provide some insight into the link between diet soda consumption and obesity.

Nonnutritive Sweeteners: Where Are We Today?

Controversy continues to surround use of nonnutritive sweeteners among consumers, despite extensive premarket safety studies used in the rigorous approval process of the U.S. Food and Drug Administration (FDA). The American Diabetes Association and the National Cancer Institute hold positions that FDA-approved nonnutritive sweeteners may be safely used by consumers.1 However, people with diabetes also continue to question the use of nonnutritive sweeteners in a diabetes eating plan even with this assurance. Misinformation regarding nonnutritive sweeteners is shared routinely through multiple sources such as the Internet, print media, and electronic communications. As a result, diabetes educators and other health care professionals need to become more familiar with the safety and usage of these products to help people with diabetes discern fact from fiction. The potential benefits of nonnutritive sweeteners for people with diabetes are reductions in calories and carbohydrates for weight management and glycemic control, respectively, as well as reductions in the risk of tooth decay.2 This article reviews the history of nonnutritive sweeteners, explains FDA safety standards and definitions, and provides an overview of nonnutritive sweeteners available in the United States and practical teaching tips for counseling consumers about their use. Sweetening agents are broadly classified as nutritive sweeteners, which provide energy, and nonnutritive sweeteners, which provide little to no energy. Nonnutritive sweeteners are several hundred to several thousand times sweeter than sucrose. Although some actually provide calories, their intense sweetness means that they are used in such small amounts that they are generally considered noncaloric. Familiar nutritive sweeteners include sucrose, fructose, agave nectar, fruit juice, and honey. Each provides ~ 4 kcal/g. Nonnutritive sweeteners are different from sugar alcohols (also known as polyols) such as xylitol and sorbitol, which are considered nutritive sweeteners, providing an average of 2 kcal/g because of their incomplete digestion and absorption. …

Position of the Academy of Nutrition and Dietetics: Use of Nutritive and Nonnutritive Sweeteners

It is the position of the Academy of Nutrition and Dietetics that consumers can safely enjoy a range of nutritive sweeteners and nonnutritive sweeteners (NNS) when consumed within an eating plan that is guided by current federal nutrition recommendations, such as the Dietary Guidelines for Americans and the Dietary Reference Intakes, as well as individual health goals and personal preference. A preference for sweet taste is innate and sweeteners can increase the pleasure of eating. Nutritive sweeteners contain carbohydrate and provide energy. They occur naturally in foods or may be added in food processing or by consumers before consumption. Higher intake of added sugars is associated with higher energy intake and lower diet quality, which can increase the risk for obesity, prediabetes, type 2 diabetes, and cardiovascular disease. On average, adults in the United States consume 14.6% of energy from added sugars. Polyols (also referred to as sugar alcohols) add sweetness with less energy and may reduce risk for dental caries. Foods containing polyols and/or no added sugars can, within food labeling guidelines, be labeled as sugar-free. NNS are those that sweeten with minimal or no carbohydrate or energy. They are regulated by the Food and Drug Administration as food additives or generally recognized as safe. The Food and Drug Administration approval process includes determination of probable intake, cumulative effect from all uses, and toxicology studies in animals. Seven NNS are approved for use in the United States: acesulfame K, aspartame, luo han guo fruit extract, neotame, saccharin, stevia, and sucralose. They have different functional properties that may affect perceived taste or use in different food applications. All NNS approved for use in the United States are determined to be safe.

Sweeteners in the US food supply and the role of fruit juice concentrates (FJC)

Added sugars measurements defined by the USDA and estimated in MPED exclude fruit juice concentrate (FJC) as a sweetener, and have not been created since NHANES 2003/04. This study utilizes full ingredient list and nutrition facts panel (NFP) data from Gladson Nutrition Database, and nationally representative food purchases from Nielsen Homescan 2005–2009. Of the 85,452 uniquely formulated foods purchased between 2005–2009 representing >400,000 items in the marketplace, 75% contain sweeteners (73.3% nutritive, 1.3% non‐nutritive). 7% contain FJC (not reconstituted) as a sweetener, and 2% contain reconstituted fruit juice. FJC as a sweetener is used in 13% of granola or energy bars, 12% of baby food, 17% of salad dressings and dips, 18% of sweets, 11% of ready‐to‐eat cereals, 16% of yogurts, 30% caloric sugar‐ and 16% of diet‐sweetened beverages. Among uniquely formulated products, those containing FJC as the only sweetener have a mean of 21g total sugar/100g, which is not statistically different from the 23g total sugar in products sweetened only by other nutritive sweeteners. However, when total sugar/100g is weighted by volume purchased, we found that foods purchased in 2007–2008 containing FJC as the only sweetener had significantly higher total sugars than those sweetened by other nutritive sweeteners only (20.1–20.3g vs. 15.9–16.1g, p>0.05). Our study poses a challenge toward monitoring what is consumed in the US by discussing the need to improve added sugar measures and require added sugars in NFP labeling regulations. Funding for this research is from the Robert Wood Johnson Foundation (Grant 68793) and the National Institutes of Health (R01 HL104580).

Sucrose‐predictive cues evoke greater phasic dopamine release than saccharin‐predictive cues

Cues that have been paired with food evoke dopamine in nucleus accumbens (NAc) and drive approach behavior. This cue-evoked dopamine signaling could contribute to overconsumption of food. One manner in which individuals try to restrict caloric intake is through the consumption of foods containing artificial (non-nutritive) sweeteners. We were interested in whether cues paired with a non-nutritive sweetener (saccharin) would evoke similar dopamine release as cues paired with a nutritive sweetener (sucrose). We trained food-restricted rats to associate distinct cues with sucrose or saccharin pellets. In the first group of rats, training sessions with each pellet took place on different days, maximizing the opportunity for rats to detect nutritional differences. After training, voltammetry recordings in NAc core revealed that sucrose cues evoked greater phasic dopamine release than saccharin cues. In a second group of rats, on each training day, sucrose and saccharin pellets were presented in pseudorandom order within the same session, to mask nutritional differences. In this condition, the difference in dopamine between sucrose and saccharin cues was attenuated, but not abolished. These results suggest that sucrose-paired cues will more powerfully motivate behavior than saccharin-paired cues. The differing responses to each cue seem to be driven by overall preference with both the nutritional value that the pellets predict as well as other factors, such as taste, contributing.

The Australian paradox: a substantial decline in sugars intake over the same timeframe that overweight and obesity have increased.

Ecological research from the USA has demonstrated a positive relationship between sugars consumption and prevalence of obesity; however, the relationship in other nations is not well described. The aim of this study was to analyze the trends in obesity and sugar consumption in Australia over the past 30 years and to compare and contrast obesity trends and sugar consumption patterns in Australia with the UK and USA. Data on consumption of sugar in Australia, the UK and USA were obtained from the Food and Agriculture Organization for the years 1980-2003. The prevalence of obesity has increased 3 fold in Australians since 1980. In Australia, the UK and USA, per capita consumption of refined sucrose decreased by 23%, 10% and 20% respectively from 1980 to 2003. When all sources of nutritive sweeteners, including high fructose corn syrups, were considered, per capita consumption decreased in Australia (−16%) and the UK (−5%), but increased in the USA (+23%). In Australia, there was a reduction in sales of nutritively sweetened beverages by 64 million liters from 2002 to 2006 and a reduction in percentage of children consuming sugar-sweetened beverages between 1995 and 2007. The findings confirm an “Australian Paradox”-a substantial decline in refined sugars intake over the same timeframe that obesity has increased. The implication is that efforts to reduce sugar intake may reduce consumption but may not reduce the prevalence of obesity.

Two solutions in search of a problem

Two recent articles in HEPATOLOGY suggest that the problems of fructose-induced fibrosis severity in patients with nonalcoholic fatty liver disease (NAFLD)1 or nonalcoholic hepatic steatosis (NASH)2 could be solved if their exposure were limited either directly through diet or indirectly through curcumin therapy. However, the evidence for a unique fructose effect is sufficiently weak in both studies that the authors appear left with two solutions in search of a problem. The evidence of Abdelmalek et al.1 for a fructose-specific role in NAFLD is not convincing for several reasons. First, in the categorization of subjects by sweetened beverage intake, the designation “no fructose consumers” is misleading; fructose intake from nonbeverage sources was neither calculated nor reported and could have significantly altered clinical and histological conclusions. Second, the raw data in Table 1 of their article (before statistical manipulation) demonstrate inconsistent fructose dose–dependent trends for all but two of the seven metabolic parameters and for all of the histological parameters measured. Third, the caloric difference between the subject groups [the highest fructose consumers (seven or more servings per week) had twice the calorie intake of the no-fructose group (zero servings per week)] cannot be ignored as a far simpler explanation for the few observed differences reported by the authors. This is especially compelling because the fructose increment in moderate consumers versus zero consumers could not have exceeded 15% of the total energy, whereas that for the highest consumers could have been as low as 5% (calculated from Table 1 of their article). Thus, rather than proposing reduced fructose intake as the solution for NAFLD patients at risk for liver fibrosis, Abdelmalek et al. should recommend that these patients eat less of everything. The experimental design of Li et al.2 provided rats ad libitum access to 10% (wt/vol) fructose in water with or without curcumin or pioglitazone and standard rat chow. The data in Fig. 1 of their article show that the fructose rats consumed approximately 1650 mL of fluid per week (236 mL/day), which is equivalent to 94 kcal/day from fructose. For perspective, this would be like feeding a 70-kg human more than 5200 g of fructose per day (21,000 kcal/day). From the combination of such a highly exaggerated exposure and a lack of a suitable nonfructose carbohydrate control, we can conclude only that (1) this study does not prove a meaningful role for fructose in the development of hepatic steatosis at typical intake levels (45 g/day or 180 kcal/day3), and (2) the curcumin therapy solution proposed by Li et al. has academic interest but is likely unnecessary in humans. Because Abdelmalek et al.1 and Li et al.2 have failed to demonstrate a unique effect for fructose in patients with NAFLD or NASH, respectively, they are left with two solutions in search of a problem. John S. White Ph.D. Potential conflict of interest: John S. White is the president of White Technical Research and is a consultant to the food and beverage industry in the area of nutritive sweeteners. His clients include research institutes, food industry councils, trade organizations, and individual companies. John P. Foreyt is a professor of the Department of Medicine at Baylor College of Medicine and is the director of the Behavioral Medicine Research Center. He has received research funding from the National Institutes of Health and has served as a consultant to the pharmaceutical and food industries, food industry councils, trade organizations, and research institutes.*, John P. Foreyt Ph.D. , * White Technical Research, Argenta, IL, Baylor College of Medicine, Houston, TX.

Experimental evaluation of antipyretic and analgesic activity of aspartame.

Sir, It has been reported that aspartame is biologically active and appears to relieve pain and induce mild antithrombotic effects in humans, and decrease fever in animals.[1] There is, however, a paucity of data about the biological effects of aspartame, which prompted us to undertake the present study, with a view to investigate the possible antipyretic and analgesic effects of aspartame and its comparison with conventional drugs. Albino Wistar rats of either sex (age 3-4 months, weight 200 g) were used to study the antipyretic effect, while adult mice of either sex, weighing 20-30 g, were used to study the analgesic effect. The care and maintenance of animals were as per the approved guidelines and the study was approved by the Institutional Animal Ethics Committee. Aspartame was obtained from Zydus Cadila (Ahmedabad, India). The antipyretic effect was evaluated by a 2-hour test using TAB vaccine (0.3 mL, i.p.). Rectal temperature was recorded using a clinical thermometer for a period of 2 minutes, both in basal state and at 30 minutes interval for 2 hours after the administration of vaccine. The animals were divided into five groups of 10 animals each. Group I received 0.3 mL distilled water (control). Groups II, III and IV received aspartame in a dose of 2, 4 and 8 mg/kg, respectively. Group V was administrated paracetamol (220 mg/kg). The reduction in mean rise of temperature was noted. The analgesic effect was studied by acetic acid induced writhing method.[2] Mice were divided into five groups of 10 animals each. Group I received 0.3 mL distilled water (control). Groups II, III and IV received aspartame in doses of 2, 4 and 8 mg/kg, respectively. Group V was given diclofenac 1 mg/kg by intraperitoneal route, 15 minutes prior to acetic acid injection. After intraperitoneal injection of 3% aqueous acetic acid (300 mg/kg), the mice were observed under a bell jar for a period of 20 minutes and the number of writhing episodes was noted. An average value for each group was calculated and subsequently used for comparison. In addition, protection provided by the test drugs was also calculated using the formula % protection =100 –number of writhes in experimental group × 100 number of writhes in control group Table 1 shows the effect of aspartame on rectal temperature of rats following administration of TAB vaccine. Aspartame showed a statistically significant (P < 0.001) antipyretic effect at all the doses used and this was comparable with paracetamol. Table 2 shows the effect of aspartame and diclofenac on acetic acid induced writhing episodes in mice. Aspartame in doses of 4 and 8 mg/kg showed statistically significant (P < 0.01) protection against writhing. Diclofenac, a potent analgesic compound, produced highly significant (P < 0.001) effect on writhing in doses of 1 mg/kg, i.p. Table 1 Mean rise of rectal temperature (°F) in rats Table 2 Effect of aspartame and diclofenac on acetic acid induced writhing episodes in mice In our study, we found that aspartame has highly significant antipyretic effect in doses of 2, 4 and 8 mg/kg. To our knowledge, there are no published reports of experimental evaluation of antipyretic effect of aspartame in this model. We also found that in doses of 4 and 8 mg/kg, aspartame showed a significant analgesic activity. Another study has shown that oral administration of aspartame (2-16 mg/kg) significantly increased the pain threshold against acetic acid induced writhing in mice.[3] In yet another study, it has been shown that aspartame attenuates mechanical allodynia in high doses (50 mg/kg).[4] Since this study was conducted in carrageenan-induced monoarthritis model, it appears that differences in the experimental models of evaluation of analgesic activity may account for the variation in effective doses. Interference with rheumatoid factor activity has been proposed to alleviate the pain and immobility resulting from chronic inflammation of joint.[5] In the acetic acid induced writhing method, nociceptive response involves release of endogenous substrates like bradykinin and prostanoids.[6] It is speculated that the antagonism of these chemicals may underlie the pain-relieving mechanism of aspartame. However, the exact mechanism of analgesic action of aspartame can be investigated by further pharmacological studies to overcome the limitations of current work. To conclude, aspartame is an intense nutritive sweetener, which is widely used by diabetic patients and overweight persons. Our study has demonstrated an antipyretic effect of aspartame and confirmed its analgesic effect in an experimental model. Further studies on biological effects of aspartame are required to explore its therapeutic potential as an antipyretic and analgesic agent.

The State of the Science on Dietary Sweeteners Containing Fructose: Summary and Issues to Be Resolved

This article highlights the discussion of the issues that had been raised during the International Life Sciences Institute North America- and USDA Agricultural Research Service-sponsored workshop surrounding the consumption of fructose. One conclusion of the discussion was that the metabolic effects of high-fructose corn syrup (HFCS) and sucrose appear to be similar in humans. However, there have been few studies directly comparing the effects of fructose to other caloric sweeteners, such as glucose, HFCS, and sucrose. Differential effects may include those related to insulin sensitivity, triglyceride and lipoprotein levels, and glycated protein levels. Further exploration of the differences between nutritive sweeteners should be the basis of a research agenda. Studies should also further investigate factors that might affect the results, such as the amount and form of the sweetener consumed, the macronutrient composition of the basal diet, the length of the study, and the characteristics of the subjects. Meanwhile, health professionals could help consumers by providing simple messages, such as the importance of consuming lower levels of energy, including those from all caloric sweeteners.

Straight talk about high-fructose corn syrup: what it is and what it ain't

High-fructose corn syrup (HFCS) is a fructose-glucose liquid sweetener alternative to sucrose (common table sugar) first introduced to the food and beverage industry in the 1970s. It is not meaningfully different in composition or metabolism from other fructose-glucose sweeteners like sucrose, honey, and fruit juice concentrates. HFCS was widely embraced by food formulators, and its use grew between the mid-1970s and mid-1990s, principally as a replacement for sucrose. This was primarily because of its sweetness comparable with that of sucrose, improved stability and functionality, and ease of use. Although HFCS use today is nearly equivalent to sucrose use in the United States, we live in a decidedly sucrose-sweetened world: >90% of the nutritive sweetener used worldwide is sucrose. Here I review the history, composition, availability, and characteristics of HFCS in a factual manner to clarify common misunderstandings that have been a source of confusion to health professionals and the general public alike. In particular, I evaluate the strength of the popular hypothesis that HFCS is uniquely responsible for obesity. Although examples of pure fructose causing metabolic upset at high concentrations abound, especially when fed as the sole carbohydrate source, there is no evidence that the common fructose-glucose sweeteners do the same. Thus, studies using extreme carbohydrate diets may be useful for probing biochemical pathways, but they have no relevance to the human diet or to current consumption. I conclude that the HFCS-obesity hypothesis is supported neither in the United States nor worldwide.

Modeling of the Psychophysical Response Curves Using the Grand Canonical Ensemble in Statistical Physics

This paper aims to investigate the peripheral mechanism of taste perception by the use of the grand canonical ensemble in statistical physics. It allows a better understanding of this process and its interpretation at a microscopic level. The experimental part allowed us to obtain psychophysical curves relative to four nutritive sweeteners (sucrose, fructose, glucose, and maltitol). These curves represent the intensity of sweetness as a function of sugar concentration in water. A Sensory Measuring Unit for Recording Flux (SMURF) device is used to obtain intensity–time curves for each of the studied sweeteners. To model these curves we have established the expressions of some models using grand canonical ensemble formalism in statistical physics and applying some simplification approaches. The fitting of the psychophysical data with statistical models by numerical simulation demonstrates a good correlation between the models and the experimental curves. Some physicochemical parameters interfere in the expression of the established models. These parameters are classified in two categories: on one hand, the steric aspect, which is manifested by the density of taste receptor site, and the number of molecules per receptor site and on the other hand, an energetic aspect illustrated by the concentration at half saturation, which gives indirectly the sweet molecule-receptor site energy of interaction.

Effects of sucromalt on postprandial responses in human subjects

To compare postprandial responses elicited by sucromalt, a nutritive sweetener produced by treating a blend of sucrose and corn syrup with an enzyme from Leuconostoc mesenteroides, with those after 42% of high-fructose corn syrup (HFCS), and to see if the reduced responses after sucromalt could be accounted for by carbohydrate malabsorption. Three experiments were performed in separate groups of normal subjects studied after overnight fasts using double-blind, randomized, cross-over designs. HFCS was used as the control because it contained a similar amount of fructose as sucromalt. Experiment 1 (n = 10): plasma glucose and insulin were measured after 50 g sucromalt and 50 g HFCS. Experiment 2 (n = 10): metabolic profiles were measured after 80 g HFCS, 80 g sucromalt or 56 g fructose/glucose blend plus 24 g inulin. Experiment 3 (n = 20): the glycaemic indices of sucromalt and HFCS were determined. Mean glucose and insulin responses after sucromalt were 66 and 62%, respectively, of those after HFCS (P < 0.05). The inulin treatment, used to mimic the effects of carbohydrate malabsorption, elicited higher breath hydrogen (H2), lower glucose and insulin responses, and a significantly earlier rise in serum free fatty acids (FFA) than those of HFCS (all P < 0.05). Sucromalt elicited no rise in breath H2, and delayed falls in glucose and insulin, and a delayed rebound of FFA compared to HFCS (all P < 0.05). The reduced glucose and insulin responses elicited by sucromalt are not explained by malabsorption and are more likely related to differences in either rate of digestion and absorption or postabsorptive handling by body.